The Oncogenic MicroRNA miR-22 Targets the TET2 Tumor Suppressor to Promote Hematopoietic Stem Cell Self-Renewal and Transformation
Cell Stem Cell, ISSN: 1934-5909, Vol: 13, Issue: 1, Page: 87-101
2013
- 289Citations
- 277Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations289
- Citation Indexes289
- 289
- CrossRef217
- Captures277
- Readers277
- 277
Article Description
MicroRNAs are frequently deregulated in cancer. Here we show that miR-22 is upregulated in myelodysplastic syndrome (MDS) and leukemia and its aberrant expression correlates with poor survival. To explore its role in hematopoietic stem cell function and malignancy, we generated transgenic mice conditionally expressing miR-22 in the hematopoietic compartment. These mice displayed reduced levels of global 5-hydroxymethylcytosine (5-hmC) and increased hematopoietic stem cell self-renewal accompanied by defective differentiation. Conversely, miR-22 inhibition blocked proliferation in both mouse and human leukemic cells. Over time, miR-22 transgenic mice developed MDS and hematological malignancies. We also identify TET2 as a key target of miR-22 in this context. Ectopic expression of TET2 suppressed the miR-22-induced phenotypes. Downregulation of TET2 protein also correlated with poor clinical outcomes and miR-22 overexpression in MDS patients. Our results therefore identify miR-22 as a potent proto-oncogene and suggest that aberrations in the miR-22/TET2 regulatory network are common in hematopoietic malignancies.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1934590913002610; http://dx.doi.org/10.1016/j.stem.2013.06.003; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84880571480&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/23827711; https://facultyopinions.com/prime/718082661#eval793482597; http://dx.doi.org/10.3410/f.718082661.793482597; https://linkinghub.elsevier.com/retrieve/pii/S1934590913002610; http://www.cell.com/cell-stem-cell/abstract/S1934-5909(13)00261-0?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1934590913002610%3Fshowall%3Dtrue; http://www.cell.com/article/S1934590913002610/abstract; http://www.cell.com/article/S1934590913002610/fulltext; http://www.cell.com/article/S1934590913002610/pdf; http://linkinghub.elsevier.com/retrieve/pii/S1934590913002610; http://www.cell.com/cell-stem-cell/retrieve/pii/S1934590913002610?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1934590913002610%3Fshowall%3Dtrue; http://f1000.com/prime/718082661#eval793482597
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